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Aim: Because of economic inflation, different-sized coins are in circulation in our country. The coin ingestion and retention in the esophagus are common problems in childhood. We evaluated the patients with coins retained in the esophagus and the impact of the size of the coins on lodgment., Patients and Methods: Sixty-two children with a history of coin ingestion and a chest X-ray with retained coin in the esophagus were evaluated. Patients' age, sex, type of the ingested coin, and localization of coin were recorded. The size of all coins was measured. All coins were removed either directly with a Magill forceps or with the aid of an esophagoscope from the esophagus under general anaesthesia., Results: There were 27 male and 35 female patients with coin lodgment (median age, 4 years; range, 1-13). Forty-five patients (73%) ingested a coin with a diameter between 23.45 and 26.00 mm. In the remaining 17 patients (27%), the coins had a diameter between 17.00 and 20.90 mm or between 26.85 and 28.00 mm. Fifty coins were at the upper esophagus, eight coins were in the middle esophagus, and 4 patients had a coin in the distal esophagus. There was a positive correlation between the diameter of coin and age of the patient (r = 0.415 and P < 0.001)., Conclusions: Coin ingestion is rather common among childhood and its treatment may require an endoscopic approach. Most retained coins had a diameter between 23.45 and 26.00 mm. We think we could redesign our coins so that they would either be too big to ingest or so small they would always pass spontaneously.

The aim of the study reported here was to evaluate the biochemical and histopathologic effects of omeprazole and vitamin E in rats with corrosive esophageal burns. A total of 144 Wistar Albino rats were divided into 12 experimental groups (12 rats per group) and used in an animal study. Group I rats were given a laparotomy and received no treatment (control group), while groups II, III and IV received a laparotomy and were treated with omeprazole, vitamin E or omeprazole/vitamin E, respectively. Groups V-XII rats received a laparotomy and were given a caustic acid burn through acid instillation (1 ml caustic 10% sulphuric acid; groups V-VIII) or alkali instillation (corrosive 10% sodium hydroxide solution; groups IX-XII) into the isolated esophageal segment via a 22-Fr cannula for 2 min. Each group of rats subjected to caustic burn received either no treatment (groups V and IX) or were treated with omeprazole, vitamin E or omeprazole/vitamin E, respectively (remaining six groups). Omeprazole (20 mg/kg) or vitamin E (10 mg/kg) was administered to the rats intraperitoneally or intramuscularly, respectively. Seventy-two rats (50% of each group, n = 6) were killed immediately after the experimental treatment (acute phase). The remaining rats were kept under standard conditions for 21 days (late phase) before being killed. The distal esophageal segments were harvested from all animal and used in histopathologic and biochemical analyses. Compared to the controls (no caustic burn), rats receiving only the acid or alkali installation (and no subsequent treatment) had the highest mean malondialdehyde (16.9 and 15.8 micromol MDA/g protein, respectively) and hydroxyproline (5.9 and 5.7; mg HP/g wet tissue) levels of all groups. In comparison, rats treated with acid + omeprazole and/or vitamin E had relatively lower MDA (12.9 and 11.6 micromol/g protein, respectively) and HP levels (4.3 and 4.08 mg/g wet tissue, respectively). Similarly, rats treated with alkali + omeprazole and/or vitamin E had low levels of MDA (13.9 and 11.7 micromol/g protein, respectively) and HP (4.3 and 4.4 mg/g wet tissue, respectively). The glutathione (GSH) levels of acid-only- or alkali-only-treated rats were lower than those found in omeprazole- and/or vitamin E-treated rats. Based on these results, we conclude that vitamin E and omeprazole affect the biochemical and histopathologic parameters in rats receiving corrosive esophageal burn from acid and alkali. The effect of both substances was slightly greater in the acid-treated groups.

Purpose: In our country, safety pin ingestion by infants is commonplace. When swallowed, open safety pins are mostly found within the esophagus or stomach, and they cannot be easily removed by rigid esophagogastroscopy. Our aim was to evaluate the removal of safety pins using flexible endoscopy in infants., Materials and Methods: We evaluated the cases of 7 infants who had ingested open safety pins between 2001 and 2004. In all the patients, the primary diagnostic tool was a direct x-ray of the neck, chest, and abdomen. In all cases, the safety pins were removed by flexible esophagogastroduo-denoscopy. Clinical records for the cases were reviewed., Results: Four of the open safety pins were lodged in the esophagus, two in the stomach, and one in the duodenum. One infant had a safety pin lodged in the esophagus with the pin's open end pointed caudally; the pin was held with the endoscopic forceps by its tail end and removed. Three safety pins in the esophagus had their open ends pointing cephalad; these were held by their tail ends using the endoscopic forceps and pushed into the stomach. Then they were rotated in the stomach and removed tail end first. The safety pins located in the stomach or duodenum were also removed similarly. All safety pins were successfully removed, and there were no operative complications., Conclusion: Open surgery or other invasive removal methods are not necessary in infants with open safety pin ingestions. In our opinion, the best way to extract an open safety pin from the esophagus, stomach, or duodenum is by using a flexible endoscopic device.

The effects of sex hormones on the synthesis of collagen were investigated in rats with alkali-induced corrosive esophageal burns. In 75 rats, a standard esophageal burn was produced as described by Gehanno. The animals were then grouped as follows: controls (group A), animals with pure esophageal burns (group B), and animals with esophageal burns treated with estradiol and progesterone (group C). All animals were killed on the 28th day of the experiment. Hydroxyproline levels were determined, and histopathologic evaluation was performed for each group. The hydroxyproline levels were significantly lower in the rats treated with estradiol and progesterone. Histopathologically, collagen deposition in the submucosa and tunica muscularis was lower in the estradiol/progesterone group than in the group with pure esophageal burns. Based on the results, the authors believe that estradiol and progesterone inhibited new collagen synthesis, and therefore, alkali-induced esophageal stricture formation.